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1 molecule could be a novel approach to treat allergic asthma.
2 mmunomodulatory approach to the treatment of allergic asthma.
3 ouse model of severe exacerbation of chronic allergic asthma.
4 +) T cells are critical for the induction of allergic asthma.
5 e assessed in a murine model of experimental allergic asthma.
6 and airways resistance in a murine model of allergic asthma.
7 helium-specific ERp57 in the pathogenesis of allergic asthma.
8 HDM) is a risk factor for the development of allergic asthma.
9 kin allergen responses in patients with mild allergic asthma.
10 nal role of 17q12-21 in patients with AR and allergic asthma.
11 jor signalling centre in the pathogenesis of allergic asthma.
12 ation, associated with poor lung function in allergic asthma.
13 tion of biomarkers for allergic rhinitis and allergic asthma.
14 B cells and Tfh cells in the pathogenesis of allergic asthma.
15 cepsilonRI expression in a clinical model of allergic asthma.
16 to allergens and is an important mediator of allergic asthma.
17 us) during the inception and exacerbation of allergic asthma.
18 kinase, may represent a novel treatment for allergic asthma.
19 n/interventional strategies for treatment of allergic asthma.
20 rgen-induced responses in subjects with mild allergic asthma.
21 s may be very effective for the treatment of allergic asthma.
22 erved in Citrobacter rodentium infection and allergic asthma.
23 erleukin 13, is used as treatment for severe allergic asthma.
24 ring the role of CD39 expression by Tregs in allergic asthma.
25 nd enhances susceptibility to a TH2 model of allergic asthma.
26 ically present in atopic diseases, including allergic asthma.
27 us production during house dust mite-induced allergic asthma.
28 crobiome for the treatment and prevention of allergic asthma.
29 K may be a potential target for treatment of allergic asthma.
30 a significant cause of allergic rhinitis and allergic asthma.
31 can ameliorate inflammatory diseases such as allergic asthma.
32 after allergen provocation in patients with allergic asthma.
33 ons in circulating PBMCs are associated with allergic asthma.
34 l responses and promoting the development of allergic asthma.
35 te matter (PM) contribute to exacerbation of allergic asthma.
36 are the primary antigen-presenting cells in allergic asthma.
37 f NSC23766 prevented AHR in murine models of allergic asthma.
38 ns of vitamin E isoform gamma-tocotrienol in allergic asthma.
39 Tfh cells that results in protection against allergic asthma.
40 o mice with already established experimental allergic asthma.
41 therapeutic intervention for the control of allergic asthma.
42 cted against IgE can alleviate hay fever and allergic asthma.
43 ucocorticosteroid reduction in patients with allergic asthma.
44 IL-4 and IL-13 play a crucial role during allergic asthma.
45 the potential for Breg-targeted therapies in allergic asthma.
46 mechanisms of IT in a mouse model of chronic allergic asthma.
47 important for initiation and progression of allergic asthma.
48 Cs), which can be deficient in patients with allergic asthma.
49 ential to be used as a therapeutic option in allergic asthma.
50 LP) on Treg frequency using a human model of allergic asthma.
51 was sufficient to mediate protection against allergic asthma.
52 TLR3 triggered exacerbation of experimental allergic asthma.
53 o the lung and the subsequent development of allergic asthma.
54 (>/=12 years of age) with moderate-to-severe allergic asthma.
55 the relevance of glycolysis in patients with allergic asthma.
56 nhibitors may be used as novel therapies for allergic asthma.
57 neous immunotherapy for birch pollen-induced allergic asthma.
58 n transcripts of PBMCs from 10 children with allergic asthma.
59 evalent and clinically important triggers of allergic asthma.
60 Grail-deficient mice are more susceptible to allergic asthma.
61 nate receptor NOD1 have been associated with allergic asthma.
62 f the enhanced susceptibility for TH2-driven allergic asthma.
63 dust mite allergens in 15 patients with mild allergic asthma.
64 ined whether BATF expression would influence allergic asthma.
65 s that forge the IgG4 and IgE repertoires in allergic asthma.
66 sistent airway inflammation in patients with allergic asthma.
67 he treatment of allergic diseases, including allergic asthma.
68 ubset and is implicated in the mechanisms of allergic asthma.
69 esent effective targets for the treatment of allergic asthma.
70 te the role of TGF-beta1 in MSC migration in allergic asthma.
71 Here we tested the role of EP2 signaling in allergic asthma.
72 is a known risk factor for individuals with allergic asthma.
73 lammation and remodeling in a mouse model of allergic asthma.
74 al as an adjunct therapy in the treatment of allergic asthma.
75 consistent with omalizumab in patients with allergic asthma.
76 We used an OVA-induced experimental model of allergic asthma.
77 2 responses contribute to the development of allergic asthma.
78 ovel therapeutic target for the treatment of allergic asthma.
79 lar lavage fluid (BALF) in a murine model of allergic asthma.
80 in patients with mild-to-moderate persistent allergic asthma.
81 tion of atopic dermatitis, food allergy, and allergic asthma.
82 n the development and molecular pathology of allergic asthma.
83 ant allergen sources and a major elicitor of allergic asthma.
84 olerogenic effects in experimentally induced allergic asthma.
85 flammation, which is central to eosinophilic allergic asthma.
86 onses and IgE formation in a murine model of allergic asthma.
87 hold promise for prevention or treatment of allergic asthma.
88 infection and conferring protection against allergic asthma.
89 PARP-14 might be a potential new therapy for allergic asthma.
90 with proved efficacy in patients with severe allergic asthma.
91 okine levels was determined in children with allergic asthma.
92 or influenza infection on the development of allergic asthma.
93 is not known to modulate the pathogenesis of allergic asthma.
94 ddress its importance in the pathogenesis of allergic asthma.
95 ibody, is used to treat patients with severe allergic asthma.
96 through the skin and can provoke features of allergic asthma.
97 and eosinophilia) in a mouse model of severe allergic asthma.
98 agonists in mitigating multiple features of allergic asthma.
99 allergens are a common cause of allergy and allergic asthma.
100 iratory epithelia might provide insight into allergic asthma.
101 y trafficking of eosinophils in experimental allergic asthma.
102 igate its involvement in AHR associated with allergic asthma.
103 asis and initiate pathologic inflammation in allergic asthma.
104 and is associated with allergic rhinitis and allergic asthma.
105 lso provide proof for a beneficial effect in allergic asthma.
106 ic target in the treatment and prevention of allergic asthma.
107 can be a risk factor for the development of allergic asthma.
108 ls in the regulation of hallmark features of allergic asthma.
109 ated influences on the overall prevalence of allergic asthma.
110 ergen-driven TH2 responses, promoting severe allergic asthma.
111 may be a successful therapeutic strategy for allergic asthma.
112 ouse model of severe exacerbation of chronic allergic asthma.
113 f rhinovirus (RV) illnesses in children with allergic asthma.
114 .03); the opposite pattern was suggested for allergic asthma.
115 subjective burden of illness chain of severe allergic asthma.
116 brosis, maladaptive vascular remodeling, and allergic asthma.
117 t present important contributing features of allergic asthma.
118 tion in T cells from pediatric patients with allergic asthma.
119 reatment available for allergic rhinitis and allergic asthma.
120 il function and its role in a mouse model of allergic asthma.
121 Among 235 high DEP-exposed children with allergic asthma, 32.2% had more frequent asthma symptoms
123 itic cells (mDCs) contribute to inception of allergic asthma (AA) and are regulated by epithelial-der
125 ide specific recommendations on treatment of allergic asthma (AA) caused by HDM allergy, although som
126 In the United States, the prevalence of allergic asthma (AA) is inexplicably rising and in utero
127 e treatment of moderate-to-severe persistent allergic asthma (AA) that remains uncontrolled despite h
131 ds and bronchial biopsies from patients with allergic asthma after allergen challenge, where it corre
132 cerbations) study, we examined children with allergic asthma (aged 6-17 yr; n = 478) from low-income
134 this study, we showed that the induction of allergic asthma alters the homeostasis of IL-10(+) Bregs
137 We showed that experimental HDM-induced allergic asthma and food allergy and anaphylaxis to pean
138 in respiratory epithelia are associated with allergic asthma and gene expression changes in inner-cit
139 ng IgE, is an established therapy for severe allergic asthma and has shown efficacy in chronic sponta
140 al cause of allergic rhinoconjunctivitis and allergic asthma and has the potential to alter the natur
141 ic rhinitis (AR), atopic dermatitis (AD) and allergic asthma and improved treatment options are neede
142 sinophils are critical cellular mediators in allergic asthma and inflammation; however, the signals t
145 , safe therapeutic tool for the treatment of allergic asthma and other diseases driven by an imbalanc
146 tile targets for prevention or management of allergic asthma and other diseases in which adaptive imm
148 r developing artesunate for the treatment of allergic asthma and other mast cell-mediated allergic di
149 ther elucidating a role for this molecule in allergic asthma and potentially other eosinophilic disor
153 important source of indoor allergens causing allergic asthma and rhinitis in tropical and subtropical
154 otherapy (AIT) is an effective treatment for allergic asthma and rhinitis, as well as venom-induced a
156 ether glycolysis is altered in patients with allergic asthma and to address its importance in the pat
157 sive panel of HDM allergens in children with allergic asthma and to compare them with those of nonast
158 in the sensitization and effector phases of allergic asthma and to determine the chemokine receptors
159 tially regulated both in murine and in human allergic asthma and were associated with clinical charac
160 (>/=12 years of age) with moderate to severe allergic asthma and who were being treated with omalizum
161 topic dermatitis, IgE-mediated food allergy, allergic asthma, and allergic rhinitis that begins with
162 ophysiologic responses seen in children with allergic asthma, and BATF has emerged as a novel target
163 vivo relevance was examined in experimental allergic asthma, and the mechanisms were assessed using
165 human nasal cells and used murine models of allergic asthma, as well as primary mouse tracheal epith
166 ases, including ischemia/reperfusion injury, allergic asthma, autoimmune nephritis, and rheumatoid ar
170 o modulate sensitization during experimental allergic asthma, but the specific role of prostaglandin
171 players in the induction and maintenance of allergic asthma by cross-linking innate and adaptive imm
172 ation of exogenous Sema3E protects mice from allergic asthma by reducing eosinophilic inflammation, s
173 ation was elicited in participants with mild allergic asthma by segmental allergen challenge before a
174 Thus, Pglyrp1(-/-) mice efficiently control allergic asthma by upregulating pDC and Treg cells in th
175 rkers to become part of allergic rhinitis or allergic asthma classifiers with high prognostic value.
177 ges superimposed on established experimental allergic asthma constitute a useful exacerbation model.
179 lly relevant asthma phenotypes: eosinophilic allergic asthma, eosinophilic nonallergic asthma and non
182 Additionally, high DEP-exposed children with allergic asthma had nearly 6 times higher serum IL-17A l
183 ertain gut microbiota and the development of allergic asthma has been shown in experiments conducted
184 owever, expression and function of Sema3E in allergic asthma has not been extensively investigated.
189 helper (Th)-2 cells are the major players in allergic asthma; however, the mechanisms that control Th
190 IT) for the management of allergic rhinitis, allergic asthma, IgE-mediated food allergy and venom all
192 ental influence on both epigenetic marks and allergic asthma in children, the epigenetic alterations
194 have recently been identified as inducers of allergic asthma in human subjects and mice, but their me
195 ells and their cytokines are associated with allergic asthma in human subjects and with mouse models
196 nic-cytidylic) acid exacerbated experimental allergic asthma in mice as characterized by enhanced rel
200 uring pregnancy may cause the development of allergic asthma in the offspring by inhibiting the endot
202 at alone causes no inflammation, exacerbates allergic asthma in young animals and suggests the import
206 rimary outcome), typical asthma symptoms, or allergic asthma (including positive IgE measurements).
207 ntly inhibited all hallmarks of experimental allergic asthma, including airway hyperreactivity, eosin
208 er of genes related to allergic rhinitis and allergic asthma increases steadily; however, prognostic
209 ate the expression of IL-31RA in vivo during allergic asthma induced by soluble egg antigen, which ma
211 In contrast, deficiency of IL-13 prevented allergic asthma, irrespective of the presence or absence
234 Although eosinophilic inflammation typifies allergic asthma, it is not a prerequisite for airway hyp
235 aling is critical during the early phases of allergic asthma, its role is much more limited once dise
236 present the severity spectrum of early-onset allergic asthma, late-onset severe asthma, and severe as
237 gs of a murine model of ovalbumin-challenged allergic asthma, leading to improved lung mechanics.
239 oal was to delineate a mechanism(s) by which allergic asthma may alleviate influenza disease outcome,
240 viding a novel mechanism by which hosts with allergic asthma may be protected from influenza morbidit
242 erties of cysteinyl leukotrienes (cysLTs) in allergic asthma mediate their effects predominantly thro
243 ir proteins, and apoptosis in an HDM-induced allergic asthma model and in lung samples from asthmatic
245 prisingly, in contrast to our findings in an allergic asthma model, we found that the severity of hyp
247 patients with persistent moderate-to-severe allergic asthma not sufficiently controlled on standard
254 , and remodeling as pathological features of allergic asthma provoked by house dust mite in vivo.
255 Subsequently, six non-smoking men with mild allergic asthma received single doses of RPL554 (three r
256 insufficiently controlled moderate-to-severe allergic asthma receiving standard inhaled glucocorticos
258 nscripts in the circulation of children with allergic asthma reflect some characteristics of classica
261 ons between IgE levels and allergic disease (allergic asthma, rhinitis, and eczema) and between alcoh
264 YKL-40 and CHIT1 bioactivity are enhanced in allergic asthma subjects after segmental allergen challe
267 ify Sema3E as a novel regulatory molecule in allergic asthma that acts upstream of proallergic events
268 est is a long-standing exacerbation model of allergic asthma that can induce several clinical and pat
269 ies of omalizumab in the treatment of severe allergic asthma that included 4117 unique patients from
270 nknown mode of GC action in the treatment of allergic asthma that might help to develop more specific
272 s study unveil a deleterious role of NOD1 in allergic asthma through direct induction of CCL17 by den
273 r IL-13 antagonist as therapeutic agents for allergic asthma through expanding LV mediated-enhanced a
274 airway epithelium and used murine models of allergic asthma to evaluate the relevance of epithelium-
275 , we randomly assigned 31 patients with mild allergic asthma to receive three monthly doses of AMG 15
278 data represent a novel approach to treating allergic asthma via regulation of immune response to hou
279 of acute and chronic ovalbumin (OVA)-induced allergic asthma was assessed weekly in CD4(+) T cell-spe
283 mportantly, using a humanized mouse model of allergic asthma, we demonstrate that adoptive transfer o
286 ry nasal epithelial cells from patients with allergic asthma were found to express increased DUOX1 an
289 , adaptive study, and then ten men with mild allergic asthma were randomly assigned to receive placeb
290 avage eosinophils, key cells associated with allergic asthma, were increased in abr(-/-) mice, but ad
292 . pylori persistence, and protection against allergic asthma, which is a hallmark of H. pylori-infect
293 ore severe IgE-mediated disorders, including allergic asthma, which is driven by the priming of Th2 e
294 xins on Th2 and Th17 cell development during allergic asthma with a particular emphasis on their role
295 Omalizumab is licensed for therapy in severe allergic asthma with an effect demonstrated after 8 week
296 uster 4 identified patients with early-onset allergic asthma with low lung function and eosinophilic
297 the severity spectrum from mild-to-moderate allergic asthma with minimal or eosinophil-predominant s
298 7) subjects had mild-to-moderate early-onset allergic asthma with paucigranulocytic or eosinophilic s
299 al trial of SB010 involving patients who had allergic asthma with sputum eosinophilia and who also ha
300 changes that occur during the development of allergic asthma without genetic and environmental confou
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